Mingyi Xie
University of Florida, FL·Biochemistry
Cells constantly adjust how much of each gene's product they make, and a large part of that tuning is done by short RNA molecules and by chemical marks placed on RNA. MicroRNAs are tiny RNAs that latch onto messenger RNAs — the working copies of genes — and block them from being turned into protein.
- Fields
Biochemistry
Genetics
Biology
- Topics
microRNA
miRNA
Dicer
- Grants
- 3 known grants, through Jun 2028
What they work on
- Map where the m6A methyl tag sits on 7SK, a small nuclear RNA that brakes gene transcription, using a real-time PCR-based detection assay, and identify the enzymes that add and remove it by short hairpin RNA knockdown in lung cancer cells.
- Test whether removing the m6A mark from 7SK slows non-small cell lung cancer growth, using a dCasRx–ALKBH5 fusion that strips methyl groups from a chosen RNA, with proliferation, migration and soft agar colony formation assays.
- Determine how m6A changes 7SK's folded structure and its control of RNA Polymerase II, combining SHAPE-MaP structure probing with nascent RNA sequencing, Polymerase II ChIP-seq and ChIRP-seq of 7SK.
- Define how BIM messenger RNA, switched on by the steroid dexamethasone, triggers destruction of the cancer-promoting microRNAs miR-221 and miR-222 in T-cell acute lymphoblastic leukemia cells.
- Test whether degradation of miR-221/222 makes T-ALL cells more likely to die during glucocorticoid chemotherapy, and profile target-directed microRNA degradation events genome-wide in T-ALL patient samples.
- Adapt CLASH, a biochemical and bioinformatic pipeline that captures microRNAs paired with their targets, for model organisms to find conserved triggers of target-directed microRNA degradation and test which sequence and structural features make a trigger effective.
- Determine why individual microRNAs respond differently to loss of Dicer, the enzyme that cuts precursor microRNAs, using an HCT116 colorectal cancer line with doxycycline-tunable Dicer plus in vitro cleavage assays and microRNA-binding protein identification.
More about the research
Separately, RNA molecules can carry chemical tags that change how they fold and function. In cancer cells both systems go wrong: microRNA levels are abnormal, and RNA tagging is misplaced. Work in this lab asks how cells normally control the amount of each microRNA, how messenger RNAs can turn the tables and destroy the microRNAs that target them, and how one particular RNA chemical mark rewires gene expression in lung cancer.
Why it matters
Non-small cell lung cancer and T-cell acute lymphoblastic leukemia both need better treatments, and resistance to the steroid dexamethasone is a major obstacle in childhood leukemia therapy. Learning how a chemical mark on 7SK RNA drives lung cancer gene expression, and how messenger RNAs destroy cancer-promoting microRNAs during chemotherapy, could reveal targets for drugs that work by resetting RNA modifications or microRNA levels, and may explain why some patients stop responding to steroids.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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Erinn Rankin
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Test whether FTO, an enzyme that removes m6A chemical tags from RNA, drives glutamine rewiring in VHL-deficient kidney cancer by raising levels of SLC1A5, the protein that imports glutamine into cells.
Yunsun Nam
University of Texas Southwestern Medical Center, TX·Biochemistry
Determine how heavy metals alter the efficiency and specificity of METTL3-METTL14, the enzyme that adds m6A marks to mRNA, and how metal-driven m6A changes link to chromatin and DNA methylation.
The school
University of Florida: 65 labs on PI Pages, $1.3B a year on research, 795 research doctorates a year.
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